It is the objective of this study to characterize the systemic and regional hemodynamics of a model of early left ventricular failure in which left atrial pressure is elevated by hydraulic constriction of the ascending aorta. Experiments conducted under program project HL13330 have indicated that the model is feasible and investigation conducted under the aegis of this research grant Hl24503 have demonstrated small reductions in cardiac output, arterial blood pressure and renal blood flow with minimal change in total peripheral resistance and renal vascular resistance. Blockade of vagus nerves bilaterally within the neck has demonstrated that a depressor response probably mediated by cardiac receptors with vagal afferents participates in these hemodynamic changes. In acute preparations skin, muscle, gastrointestinal and renal vascular beds dialate when left atrial pressure is elevated. In contrast constriction of these vascular beds occurs with congestive heart failure when cardiac output is depressed. Characterization of the hemodynamics in these beds in this model of left ventricular failure will provide an opportunity to extend the observations on the flow distribution to intact unanesthetized animals. The model will provide a preparation in which to demonstrate the ability of a left ventricular assist device to restore normal flow distribution. Assist devices designed to aid a failing left ventricle are preload sensitive and are unable to pump more than a fraction of the cardiac output when they fill at normal left atrial pressure. Experiments will be conducted in calves which will probably be jersey calves because of their relatively slow growth. Each calf will serve as its own control prior to the experimental interventions. Blood flow will be measured by implanted electromagnetic flow probes, catheters will be implanted for pressure and flow measurements and for infusions. Aortic constriction will be performed with an implanted hydraulic occluder. Exercise and pulmonary stenosis will be added to the rest and left ventricular failure conditions without and with physical and pharmacologic interruption of the reflexes.